BK viremia and polyomavirus nephropathy in 352 kidney transplants; risk factors and potential role of mTOR inhibition

Johannes Jacobi,Alexander Weidemann,Maike Büttner,Kerstin U Amann,Antonina Prignitz,Christoph May,Karl F Hilgers,Bernd Wullich,Antje Knöll,Klaus Korn,Joachim Velden,Kai-Uwe Eckardt,Katharina Heller

doi:10.1186/1471-2369-14-207

Johannes Jacobi, Alexander Weidemann + Show 11 more

Open Access

https://doi.org/10.1186/1471-2369-14-207

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Abstract

BackgroundPolyomavirus BK nephropathy (PyVAN) remains an important cause of early graft dysfunction and graft loss in kidney transplantation.MethodsIn this retrospective, single centre cohort study we studied the incidence and outcome of BK viral infection in 352 patients transplanted in 2008–2011.ResultsDuring follow-up viral replication was detected in 48 patients (13.6%); 22 patients (6.2%) had biopsy proven PyVAN.In multivariate logistic regression analyses risk factors for BK-viremia were lack of enrolment into randomized controlled trials (RCTs), biopsy proven acute rejections, cytomegaly virus (CMV) serostatus of both donor and recipient and previous transplantation.In patients without PyVAN reduction or switch of immunosuppression was associated with rapid viral clearance and stable graft function. In contrast, in most patients with PyVAN graft function deteriorated and 5 patients prematurely lost their allograft. Switch of immunosuppression to a low dose cyclosporine plus mTOR inhibitor based regimen in patients with PyVAN was safe, well tolerated and tended to be associated with a better short-term outcome in terms of graft function compared to reduction of existing immunosuppression alone.ConclusionsWith the lack of licensed anti-polyoma viral drugs reduction or conversion of immunosuppression remains the mainstay of therapy in patients with PyVAN. The combination of low dose cyclosporine plus mTOR inhibition appears to be safe and warrants further investigation.

Highlights

Polyomavirus Polyoma virus (BK) nephropathy (PyVAN) remains an important cause of early graft dysfunction and graft loss in kidney transplantation
Renal damage caused by BK virus comprises progressive tubulointerstitial nephritis and ureteral stenosis with a considerable risk of subsequent graft failure in 15-50% of cases [8,9]
Mean follow-up was 22.2 ± 13.9 months and did not differ between different subgroups treated for BK viral infection

Summary

Introduction

Polyomavirus BK nephropathy (PyVAN) remains an important cause of early graft dysfunction and graft loss in kidney transplantation. Recent advances in transplant immunology have led to improved allograft and patient survival following solid organ transplantation. Among solid organ transplant recipients it is largely restricted to kidney transplantion. In this group of patients the prevalence of viruria, viremia and PyVAN is as high as 30, 13, and 8%, respectively [7]. It is still under debate whether reactivation of latent BK virus is host or donor-derived. Renal damage caused by BK virus comprises progressive tubulointerstitial nephritis and ureteral stenosis with a considerable risk of subsequent graft failure in 15-50% of cases [8,9]

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